Journal
MOLECULES
Volume 25, Issue 23, Pages -Publisher
MDPI
DOI: 10.3390/molecules25235717
Keywords
acute kidney injury; sepsis; apamin; lipopolysaccharide; oxidative stress; apoptosis; inflammation
Funding
- Basic Science Research Program through the National Research Foundation of Korea (NRF) - Ministry of Science and ICT and Future Planning (MSIP) [NRF-2020R1C1C1003348]
- Cooperative Research Program for Agriculture Science and Technology Development, Rural Development Administration, Republic of Korea [PJ01316601]
- Daegu Catholic University Medical Center [2020-10]
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Sepsis is the major cause of acute kidney injury (AKI) in severely ill patients, but only limited therapeutic options are available. During sepsis, lipopolysaccharide (LPS), an endotoxin derived from bacteria, activates signaling cascades involved in inflammatory responses and tissue injury. Apamin is a component of bee venom and has been shown to exert antioxidative, antiapoptotic, and anti-inflammatory activities. However, the effect of apamin on LPS-induced AKI has not been elucidated. Here, we show that apamin treatment significantly ameliorated renal dysfunction and histological injury, especially tubular injury, in LPS-injected mice. Apamin also suppressed LPS-induced oxidative stress through modulating the expression of nicotinamide adenine dinucleotide phosphate oxidase 4 and heme oxygenase-1. Moreover, tubular cell apoptosis with caspase-3 activation in LPS-injected mice was significantly attenuated by apamin. Apamin also inhibited cytokine production and immune cell accumulation, suppressed toll-like receptor 4 pathway, and downregulated vascular adhesion molecules. Taken together, these results suggest that apamin ameliorates LPS-induced renal injury through inhibiting oxidative stress, apoptosis of tubular epithelial cells, and inflammation. Apamin might be a potential therapeutic option for septic AKI.
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